i102 Dietary components influencing inflammation

Abstract

Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing and tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Components of foods can contribute directly to inflammation: for example, there may be active immune-inflammatory responses to food components, as seen in food allergies and celiac disease. Oxidised components of foods, induced through processing or cooking, may also trigger inflammation, perhaps through induction of oxidative stress. Food components can also influence inflammation through modulation of inflammatory responses. For example, antioxidants reduce activation of nuclear factor kappa B. Omega-3 fatty acids decrease production of pro-inflammatory eicosanoids (e.g. prostaglandins) and they also give rise to potent pro-resolution lipid mediators (e.g. resolvins). Certain phytochemicals also have anti-inflammatory activities, mostly demonstrated in vitro. The actions of these food components suggest that diet may have a role in influencing the risk of developing inflammatory disease, although it is more likely that diet could regulate disease severity and the rate of disease progression. These ideas have been tested in model systems (cell culture, animal models etc.), through human epidemiology and case control studies, and through interventions. Human studies investigating the nutritioninflammation axis have been conducted in healthy people and in different patient groups (e.g. people with RA). In general, healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables, fruits, nuts and fish are all associated with lower inflammation. Among individual dietary components vitamins C and E, carotenoids and omega-3 fatty acids have been associated with less inflammation. High dose omega-3 fatty acids have been used in a number of RCTs in RA. Systematic reviews and meta-analyses support that omega-3 fatty acids reduce pain and have other clinical benefits. An adversely altered gut microbiota is also linked to inflammation and there are suggestions that promoting a healthy gut microbiota might benefit people with inflammatory conditions. However the precise meaning of a healthy gut microbiota is not yet clear.